Animal models of emphysema to date have been useful but crude. They have utilized intratracheal instillation of papain, elastase or leucocyte elastase extracts which while useful to indicate mechanism are not realistic in terms of the type of injury inflicted and the activation of host responses. The study of the effects of NO2 exposure on the dynamics of collagen and elastin in the lung and on the alveolar macrophages which are believed to secrete the enzymes responsible for the initiation and persistence of any alteration which these insoluble tissue proteins will provide a more realistic approach to the study of physiologic and pathologic events occurring within the lung during injury. Prolonged NO2 exposure has been reported to induce tissue changes and physiological alteration which resemble those found in human emphysema. We believe that an understanding of the dynamic events in collagen adn elastin metabolism in the lung and the elastase and collagenases generated by alveolar macrophages during the NO2 exposure will give realistic insight into injury and repair mechanisms.